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Page 4 of 16 Burke. Plast Aesthet Res 2020;7:59 I http://dx.doi.org/10.20517/2347-9264.2020.154

Ninety-five percent of our daily UV exposure is UVA (λ = 320-450 nm) which, unlike UVB, is not filtered
by glass and does not vary seasonally in intensity. Like UVB, UVA exposure results in “signature mutations”
[6]
with T → G transversions and formation of specific pyrimidine dimers . UVA generates ROS with
resultant DNA mutations, in particular oxidation of guanosine to 8-hydroxy-deoxyguanosine (8-OHdG).
UVA penetrates the skin more deeply than does UVB: UVA reaches the epidermal stem-cell rich basal layer
and the dermis to inactivate the tumor suppressor p53 gene and to decrease immune functions so that early
skin cancers are not recognized. Only extremely high exposure to UVA might directly initiate skin cancer,
while the lower doses of UVA to which we are exposed do inhibit the normal immune response so that
UVB-initiated skin carcinomas proliferate unchecked. Furthermore, it is UVA that activates dermal matrix
metalloproteinases (MMP) to degrade collagen and elastic tissue, resulting in the wrinkled, crepe-like, and
saggy quality of photo-damaged skin.

High-energy visible blue light
Of the solar radiation that reaches the earth’s surface, 39% is visible light (VL, with λ = 400-700 nm) with
the high-energy VL in the low wavelength range (blue light). We are exposed to the high-energy VL not
[7]
only from sunlight but also from computer screens and smart phones! Early observations by Kollias et al.
showed that VL does induce skin pigmentation that can last for 10 weeks. Further research demonstrated
by exposure to a xenon-mercury lamp, that VL (up to 470 nm) induces IPD, as does UVA-I . The peak
[8]
IPD response is at wavelengths λ = 300-500 nm, including all UVA-II (λ = 320-340 nm), UVA-I (λ = 340-
[9]
400 nm), and visible blue light (λ = 400-500 nm) . This tanning (with erythema) was only seen in dark-
skinned individuals of Fitzpatrick skin type IV-VI, probably because of the large amount of melanin
in their skin; light-skin type I individuals showed no tanning after VL exposure . The corresponding
[10]
coinciding erythema may be because as melanin absorbs VL, thereby generating heat to cause vasodilation.
More exposure to VL leads to darker and more sustained pigmentation as seen also in UV-induced post-
inflammatory hyperpigmentation.

Exposure of human skin equivalents to VL has been shown in vitro and in human skin ex vitro to generate
ROS leading to induction of pro-inflammatory cytokines and MMP-1 and MMP-9 . Dose-dependent
[11]
generation of hydrogen peroxide was also measured after exposure to VL. Certainly this oxidative insult,
the inflammatory cascades, and the MMPs destroy dermal matrix to contribute to extrinsic photoaging.

IR solar radiation
Almost 50% of the solar energy reaching the earth’s surface is IR or heat energy: IR-A (λ = 700-1400 nm),
IR-B (λ = 1400-3000 nm), and IR-C (λ = 3000 nm - 1 mm). Solar terrestrial radiation is about 30% IR-A.
IR-B and IR-C do not penetrate deeply into the skin, but they do contribute to heating the skin. Direct
sunlight can raise the temperature of human skin from 37 °C to 40 °C, with darker skin types IV-VI
responding to IR exposure with greater rises in temperature than experienced by light-skinned individuals
(types I and II). Although more than 65% of incipient IR-A penetrates to the dermis and 10% to the
[12]
subcutaneous fat, normal (non-excessive) exposure does not raise the skin’s temperature .
The reaction to IR-A varies with skin type: In darker skin, melanin synthesis is stimulated with little effect
in dermal MMPs, while in lightly pigmented skin, collagen in the dermal extracellular matrix is altered not
[12]
only by destruction through activation of MMPs, but also by a direct reduction in synthesis . Thus lightly
pigmented skin manifests wrinkles and a crepe-like quality, while darkly pigmented skin responds with
increased solar lentigos - both suffering from premature extrinsic aging. In addition, chronic exposure to
IR-A induces angiogenesis and unattractive erythema ab igne as seen in “bakers’ arms” and “glassblowers’
[12]
faces” .

Although the clinical manifestations of photoaging of the skin are similar after UV and IR-A exposure, the
mechanisms of damage are different. IR-A affects the mitochondrial electron transport chain, increasing